DIABETES MELLITUS
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Transcript of DIABETES MELLITUS
By: Dr. Hala M. Al-KhalidiFaculty of Pharmacy
King Abdulaziz University2008 - 1429
New diagnostic criteria and a new classification system, treatment for diabetes mellitus
Now many new data available, more etiological information has appeared
Updates many sources- Journals, WHO reports ADA -American Diabetes Association ACE -American College of Endocrinology AACE -American Association of Clinical Endocrinology DCCT -Diabetes Control and Complications Trial (UK)
Diabetes mellitus (DM) is a group of metabolic disorders
Characterized by hyperglycemia Poor control due Insufficient insulin associated with abnormalities in CHO, fat,
& protein metabolism Resulting in chronic complications; microvascular, macrovascular, and
neuropathic disorders.
Leading cause of blindness in adults age 20- 74
End-stage renal disease. 82,000 lower extremity amputations annually. Finally, a cardiovascular event is responsible
for 75% of deaths in individuals with type 2 DM
Interventions to prevent disease in high-risk populations have been reported for type 1 and type 2
World wide epidemic of DM is alarming CDC centers predict that incidence of DM
will rise by 37.5% in the USA, developing countries 170% over the next 30 years
Type 2 DM is increasing in both adult & children
New methods of control need to be developed
by health care providers
Cost ~ $132 billion 2002, indirect costs to disability
and mortality DM lead cause of blindness, end-stage
renal disease Annual ~82,000 lower extremity
amputations Finally, a cardiovascular event in 75% of
deaths with type-2 DM
HyperglycemHyperglycemiaia
Multiple genetic Multiple genetic defectsdefects
GENETIC PREDISPOSITION
ObesityObesity
ENVIRONMENT
Deranged insulinsecretion
PRIMARY BETA-CELLDEFECT
Inadequate glucose utilization
PERIPHERAL TISSUEINSULIN RESISTANCE
HYPERGLYCEMIAHYPERGLYCEMIA
Beta-cell exhaustion
TYPE 2 DIABETESTYPE 2 DIABETES
Pathogenesis of Type 2 DMPathogenesis of Type 2 DM
TYPE 1 DIABETES TYPE 2 DIABETES
Autoimmune 10% Children &
adolescents, or any age
Rapid/complete β-cell destruction with ketoacidosis
Insulin requiring for survival
C-peptide deficient
Obesity 90% β-cell dysfunction; may
range from insulin resistance with relative insulin deficiency to a secretory defect with or without insulin resistance, or Genetic defects
Individuals Having at Least Three Components meet the Criteria for Diagnosis;
The National Cholesterol Education Program Adult Treatment Panel (NCEP-ATP) III Guidelines
FH (i.e., parents or siblings) Obesity ( ≥20% over IBW, or [BMI] ≥25
kg/m2 Physical inactivity Race or ethnicity Hypertension (≥140/90 mm Hg in adults) HDL ≤35 mg/dl and/or a TG level ≥250
mg/dL Hx. Gestational diabetes mellitus/ delivery
baby weighing >9pd’s Hx. vascular disease polycystic ovary disease. Age Common women > men
Genetic defects in insulin action Type A insulin resistance Leprechaunism Rabson-Mendenhall syndrome Lipoatrophic diabetes
Exocrine pancreas Fibrocalculous pancreatopathy Pancreatitis Trauma / pancreatectomy
Neoplasia Cystic fibrosis Haemochromatosis Endocrinopathies Cushing's syndrome Acromegaly Phaeochromocytoma Glucagonoma Hyperthyroidism Somatostatinoma
Infections Congenital rubella Cytomegalovirus Drug- or
chemical-induced
Nicotinic acid Glucocorticoids Thyroid hormone Alpha-adrenergic
agonists Beta-adrenergic
agonists
Thiazides Dilantin Pentamidine Vacor Interferon-alpha
therapy
Gestational diabetes is CHO intolerance resulting in hyperglycaemia of variable severity with onset/ first recognition during pregnancy
Definition applies irrespective of whether or not insulin is used for treatment or the condition persists after pregnancy
Symptoms of diabetes - Polyuria - Polydipsia - Unexplained weight loss - & Casual Plasma glucose conc. ≥ 200mg/dl
(11.1mmol/L)OR
Fasting Plasma Glucose ≥ 126mg/dl (7.0mmol/L)OR
2-hr postload glucose ≥ 200mg/dl (11.1mmol/L) OGTT*(only in pregnancy) *WHO 75g anhydrous glucose in
water
8hr fasting8hr fasting
A metabolic state intermediate between normal glucose homeostasis and diabetes
Not interchangeable and represent different abnormalities of glucose regulation
TEST mg/dl
NORMALIMPAIREDFASTING GLUCOSE
IMPAIREDGLUCOSE
TOLERANCE
DIABETES
MELLITUS
FASTING PLASMA GLUC.
< 110 >110 but< 126
≥126
2HR AFTER GLUC. LOAD
<140>140 but< 200≥200
RANDOM≥200 with symptoms
Hypoglycemia (Insulin Shock). Diabetic ketoacidosis (DKA). Hyperglycemic hyperosmolar non-ketotic
coma (HHNK).
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Microvasculare Diabetic Retinopathy. Diabetic Nephropathy. Diabetic Neuropathy.. InfectionMacrovascular ischmia Periphry Diabetic gangrene Heart CAD Brain CVA or TIA’s
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Near-normal glycemia will reduce the risk for microvascular and macrovascular disease complications
Ameliorate symptoms, to reduce mortality, and to improve quality of life.
Current evidence targets aggressive control
Avoid hypoglycemia and excess weight
The pancrease in a non-diabetic’s secretes small amount Insulin (basal secretion).
After meals a large amount of insulin is secreted (bouls secretion).
The goal of insulin therapy is to mimic this pattern of 24-hr glycaemic coverage.
Type-1 DM basal-bolus insulin therapy or pump therapy is successful.
Basal-bolus therapy in Type-2 DM is increasing.
Multiple oral agents, or oral agents with insulin to obtain goals.